Vomiting and gastric electrical dysrhythmia in dogs

BACKGROUND: The correlation between gastric myoelectrical activity (GMA) and gastrointestinal symptoms such as nausea and vomiting is poorly understood. The aim of this study was to assess the association of GMA with vomiting induced by retrograde gastric electrical stimulation or duodenal balloon distention. METHODS: Ten dogs were involved in this study. Vomiting was induced by retrograde gastric electrical stimulation in 6 dogs and by duodenal balloon distention in 4 dogs. Computerized spectral analysis and visual analysis were applied to detect the GMA change during various periods before and after vomiting. RESULTS: Gastric dysrhythmia preceded vomiting but was of brief duration. The major pattern of dysrhythmia immediately before vomiting was tachyarrhythmia and gastric slow wave was completely uncoupled before vomiting. Gastric dysrhythmia and slow wave uncoupling were also noticed immediately after vomiting but the dogs recovered quickly. The major pattern of dysrhythmia after vomiting was arrhythmia. GMA was normal during the periods other than 5 min before and during vomiting and 5 min after vomiting. CONCLUSIONS: Gastric dysrhythmia seems to be the cause of vomiting induced by retrograde gastric electrical stimulation or duodenal balloon distention. It is brief and characterized with tachyarrhythmia and uncoupling.     

Cisplatin-Induced Gastric Dysrhythmia and Emesis in Dogs and Possible Role of Gastric Electrical Stimulation

The aim of this study was to investigate the effect of cisplatin on gastric myoelectrical activity and the role of gastric electrical stimulation in the treatment of cisplatin-induced emesis in dogs. Seven dogs implanted with electrodes on the gastric serosa were used in a two-session study. Cisplatin was infused in both the control session and the gastric electrical stimulation session, and gastric electrical stimulation was applied in the gastric electrical stimulation session. Gastric slow waves and emesis, as well as behaviors suggestive of nausea, were recorded during each session. The results were as follows: (1) cisplatin induced vomiting and other symptoms and induced gastric dysrhythmia. The percentage of normal slow waves decreased significantly during the 2.5 h before vomiting (P = 0.01) and the period of vomiting (P < 0.001). (2) Gastric electrical stimulation reduced emesis and the symptoms score. The total score in the control session was higher than that in the gastric electrical stimulation session (P = 0.02). However, gastric electrical stimulation had no effects on gastric dysrhythmia. It is concluded that cisplatin induces emesis and gastric dysrhythmia. Gastric electrical stimulation may play a role in relieving chemotherapy-induced emetic responses and deserves further investigation.     

Long-pulse gastric electrical stimulation at tachygastrial frequency reduces food intake by inhibiting proximal gastric tone

Objective. To investigate the effects of long pulse gastric electrical stimulation (GES) at a tachygastrial frequency on food intake, gastric tone and gastric myoelectrical activity (GMA). Material and methods. Of twelve dogs implanted with electrodes and a gastric cannula, 6 underwent truncal vagotomy. Stimulus consisted of long pulses with a frequency of 9 cycles/min. Experiment one was performed in all dogs to test for food intake with or without GES. Experiment two on six normal dogs consisted of baseline, GES and recovery periods. Gastric volume and GMA were recorded. Results. 1) GES reduced food intake in both normal (398.5±111.7 g versus 573.0±97.9 g; p<0.02) and vagotomized dogs (170.6±100.4 g versus 401.0±97.3 g; p<0.05). 2) Gastric volume was increased with stimulation from 168.4±17.7 ml to 301.1±34.1 ml (p<0.02 ANOVA) and maintained at 271.8±27.6 ml. 3) The percentages of normal slow waves before, during and after GES were 83.3±4.6%, 38.0±3.5% and 61.0±12.5%, respectively (p=0.02 ANOVA). Conclusion. Long-pulse GES at tachygastrial frequency substantially reduces food intake, and is not mediated by the vagal pathway but attributed to relaxation of the stomach and impairment of intrinsic GMA.     

Early myoelectrical activity changes during gastric or duodenal ulceration in dogs

Antroduodenal myoelectric activity and gastric transmural potential difference were recorded before and during fundic, antral, or duodenal ulceration in dogs. Gastric injury was obtained by electrocoagulation of the fundic or antral mucosa. Duodenal ulceration was induced by cysteamine injection which was accompanied by nausea or vomiting. Both antral electrocoagulation and cysteamine injection were also accompanied by antral dysrhythmia and a transient decrease of the gastric transmural potential difference. Effects of antral electrocoagulation were prevented by selective vagotomy. Since antral dysrhythmia disappeared as soon as the antral or duodenal ulcers became active, ie, within three days and 24 hr respectively, it is suggested that antral dysrhythmia is the result of antroduodenal stimulation and could thus not be assessed as a criterion of active ulceration.     

Gastric electrical stimulation with short pulses reduces vomiting but not dysrhythmias in dogs

BACKGROUND & AIMS: The aim of this study was to investigate the acute effects of 3 different methods of electrical stimulation in the prevention of vasopressin-induced emetic response and gastric dysrhythmias. METHODS: Seven female hound dogs chronically implanted with 4 pairs of electrodes on gastric serosa were used in a 5-session study. Saline and vasopressin were infused in sessions 1 and 2, respectively. In the other 3 sessions with vasopressin infusion, 3 different methods of electrical stimulation (short-pulse stimulation, long-pulse stimulation, and electroacupuncture) were applied. Gastric slow waves and vomiting and behaviors suggestive of nausea were recorded in each session. In a separate study, additional experiments were performed in 5 vagotomized dogs to investigate vagally mediated mechanisms. RESULTS: Vasopressin induced gastric dysrhythmias, uncoupling of slow waves, and vomiting and behaviors suggestive of nausea (P < 0.02, analysis of variance). Long-pulse stimulation, but not short-pulse stimulation or electroacupuncture, was capable of preventing vasopressin-induced gastric dysrhythmias and gastric slow wave uncoupling. Short-pulse stimulation and electroacupuncture, but not long-pulse stimulation, prevented vomiting and significantly reduced the symptom scores, which was not noted in the dogs with truncal vagotomy. CONCLUSIONS: Long-pulse stimulation normalizes vasopressin-induced slow wave abnormalities with no improvement in vomiting and behaviors suggestive of nausea. Short-pulse stimulation and electroacupuncture prevent vomiting and behaviors suggestive of nausea induced by vasopressin but have no effects on slow waves, and their effects are vagally mediated.     

Anti-dysrhythmic effects of long-pulse gastric electrical stimulation in dogs

BACKGROUND/AIM: The aim of this study was to investigate the anti-dysrhythmic effect of long-pulse gastric electrical stimulation (GES) in dogs. METHODS: The study was performed in 7 healthy dogs implanted with 4 pairs of serosal gastric electrodes. Each dog was studied in three sessions on 3 separate days in a randomized order with recordings of gastric slow waves. In session 1 or 2, infusion of either saline or glucagon (0.1 U/kg in 20 ml saline instilled in 40 min) was given during the 2nd and 3rd 20-min periods. The protocol of session 3 was the same as that of session 2 except that GES was performed during the 2nd 20-min period. RESULTS: (1) Glucagon induced gastric dysrhythmia and decreased gastric slow-wave coupling (ANOVA, p < 0.001). The long-pulse GES normalized glucagon-induced gastric dysrhythmia and the uncoupling of slow waves. (2) Glucagon induced symptoms and behaviors suggestive of nausea and the symptoms were not improved by long-pulse GES. CONCLUSION: (1) Glucagon induces gastric dysrhythmias, slow-wave uncoupling and symptoms, and (2) long-pulse GES normalizes glucagon-induced gastric dysrhythmia and slow-wave uncoupling with no improvement in symptoms.     

Effects of muscarinic receptor stimulation and nitric oxide synthase inhibition on gastric tone and gastric myoelectrical activity in canines

Aims:  This study was designed to assess whether the muscarinic receptor stimulation and nitric oxide synthase inhibition were equally effective on gastric fundic tone or gastric myoelectrical activity (GMA) in canines, and the correlation between gastric fundic tone and GMA.
Methods:  Gastric fundic tone and GMA were recorded on seven dogs implanted with serosal electrodes and a gastric cannula.
Results:  Bethanechol and L-nitro-N-arginine (L-NNA) significantly increased gastric fundic tone; gastric volume was decreased with bethanechol or L-NNA ( P  < 0.05). Increased spike activities were observed after both bethanechol and L-NNA. The percentage of slow waves superimposed with spikes was increased with bethanechol ( P  < 0.001) and L-NNA ( P  < 0.05). There was a significant reduction in dominant frequency (DF) ( P  < 0.05), dominant power (DP) ( P  < 0.05) and percentage of normal slow waves (%N) ( P  < 0.05) with bethanechol, while no significant change was observed with L-NNA. The variation of gastric tone was not correlated with parameters of GMA.
Conclusions:  Muscarinic receptor stimulation and nitric oxide synthase inhibition have similar effects on gastric tone and gastric spike activities, but different effects on gastric slow waves. Gastric fundic tone does not correlate with gastric slow waves.     

Effects of Gastric Electrical Stimulation with Short Pulses and Long Pulses on Gastric Dysrhythmia and Signs Induced by Vasopressin in Dogs

Aims: This study was to investigate the effect of gastric electrical stimulation (GES) with short pulses, long pulses, short-pulse trains or long-pulse trains on gastric dysrhythmia and motion-sickness signs induced by vasopressin. Methods: Seven male beagle dogs implanted with four pairs of electrodes on gastric serosa were studied. The study was performed in six sessions in a randomized order. In session 1 or 2, either saline or vasopressin was infused without GES. In session 3, 4, 5 and 6, GES with short pulses, long pulses, trains of short pulses or trains of long pulses was performed before and during vasopressin infusion. Gastric slow waves and motion-sickness signs were recorded in each session. Results: (1) Vasopressin induced gastric dysrhythmia and motion sickness-like signs (ANOVA, P < 0.001). (2) GES with short pulses or trains of short pulses was capable of preventing vasopressin-induced emetic response (P < 0.001), but did not normalize gastric dysrhythmia. (3) GES with long pulses or trains of long pulses was able to normalize gastric dysrhythmia induced by vasopressin (P < 0.001), but showed no effects on vasopressin-induced motion-sickness signs. Conclusion: GES with short pulses or trains of short pulses prevents vasopressin-induced emetic response with no improvement in gastric dysrhythmia. GES with long pulses or trains of long pulses normalizes gastric dysrhythmia induced by vasopressin with no effects on signs. Xiaohua Hou and Geng-Qing Song contributed equally to this work.     

Effects of Intestinal Electrical Stimulation on Intestinal Dysrhythmia and Symptoms in Dogs

The aim of this study was to investigate the effect of intestinal electrical stimulation on small intestinal dysrhythmia and motion sickness-like symptoms induced by vasopressin. Female dogs chronically implanted with two pairs of electrodes on jejunum serosa were used in a four-session study. Saline and vasopressin were infused in sessions 1 and 2, respectively. Sessions 3 and 4 were the same as session 2, except a long- or short-pulse intestinal electrical stimulation was applied on the proximal pair of electrodes. Intestinal slow waves and motion sickness-like symptoms were recorded in each session. Results were as follows. (1) Vasopressin induced intestinal dysrhythmia, uncoupling of slow waves, and vomiting and motion sickness-like symptoms (P < 0.05, ANOVA). (2) Intestinal electrical stimulation with long pulses, but not short pulses, was capable of preventing vasopressin-induced intestinal dysrhythmia. (3) Intestinal electrical stimulation with short pulses, but not long pulses, prevented vomiting and the motion sickness-like symptoms. It is concluded that vasopressin induces intestinal dysrhythmia. Long-pulse intestinal stimulation normalizes vasopressin-induced intestinal slow-wave abnormalities with no improvement in symptoms. Short-pulse stimulation prevents emetic symptoms induced by vasopressin but has no effect on slow waves. These data suggest different mechanisms involved with different methods of intestinal stimulation.     

Inhibitory remnant stomach motility by duodenal distention after B-I gastrectomy

BACKGROUND/AIMS: Although control of gastric motility is a highly regulated process, B-I gastrectomy causes accelerated gastric emptying. We found few reports so far concerned with the mechanical effect of balloon distention of the duodenum on the remnant stomach in B-I dogs. METHODOLOGY: Four weeks after conventional distal gastrectomy with B-I reconstruction procedure, a balloon was inserted into the duodenum, and strain gauge force transducers (SGTs) were sutured onto the wall of the gastric remnant and duodenal serosa in beagles. After a two-week postoperative recovery period, gastro-duodenal motility was measured with SGTs prior to distention, during distention, and after evacuation of the balloon. The motility index (MI) was calculated every 30 minutes. RESULTS: Upon duodenal distention with 4 mL of water, motility of gastric remnant was significantly inhibited, however, no reduction in duodenal MI was observed. The response was maintained for as long as duodenal distension continued. Ninety minutes after evacuation of the balloon, MI returned to predistension levels. Increased plasma levels of cholecystokinin (CCK) were observed upon distention of the duodenal balloon. CONCLUSIONS: Motility of the remnant stomach in B-I dogs was inhibited by duodenal distension. Increased levels of plasma CCK during distention might play a role in this feedback mechanism.     

Inhibitory effects of gastric electrical stimulation on ghrelin-induced excitatory effects on gastric motility and food intake in dogs

Objective. To investigate the effects of ghrelin on food intake, gastric motility and whether gastric electrical stimulation (GES) is capable of reversing these effects of ghrelin in dogs. Material and methods. Seven healthy dogs were equipped with a gastric cannula and electrodes for the measurement of antral motility and gastric myoelectrical activity (GMA). Both food intake and gastric motility studies were performed in three sessions (control, ghrelin, 20 µg and ghrelin plus GES) in randomized order, respectively. After a 28-h fast, the animals were provided with unlimited solid food for 1.5?h, 30?min after saline or ghrelin injection. Recordings of antral contractions and GMA in each session were recorded for 30?min at baseline and 45?min after ghrelin/saline injection in the fasting state. GES was performed throughout the experiment initiated 30?min prior to the injection. Results. 1) Ghrelin significantly increased food intake from 475.6±75.5?g in the controls to 535.9±90.3?g with ghrelin (p=0.04); this excitatory effect was reversed by GES. 2) Ghrelin significantly increased the motility index from 8.6±1.6 in the controls to 16.1±2.4 with ghrelin (p=0.01) and this effect was also reversed by GES. 3). There were no effects of ghrelin on GMA. Conclusions. Ghrelin induces antral contractions and increases food intake. GES is capable of blocking these excitatory effects of ghrelin. These findings suggest that GES may inhibit the resistant effect of ghrelin on weight loss.     

Long-pulse gastric electrical stimulation at tachygastrial frequency reduces food intake by inhibiting proximal gastric tone

OBJECTIVE: To investigate the effects of long pulse gastric electrical stimulation (GES) at a tachygastrial frequency on food intake, gastric tone and gastric myoelectrical activity (GMA). MATERIAL AND METHODS: Of twelve dogs implanted with electrodes and a gastric cannula, 6 underwent truncal vagotomy. Stimulus consisted of long pulses with a frequency of 9 cycles/min. Experiment one was performed in all dogs to test for food intake with or without GES. Experiment two on six normal dogs consisted of baseline, GES and recovery periods. Gastric volume and GMA were recorded. RESULTS: 1) GES reduced food intake in both normal (398.5+/-111.7 g versus 573.0+/-97.9 g; p<0.02) and vagotomized dogs (170.6+/-100.4 g versus 401.0+/-97.3 g; p<0.05). 2) Gastric volume was increased with stimulation from 168.4+/-17.7 ml to 301.1+/-34.1 ml (p<0.02 ANOVA) and maintained at 271.8+/-27.6 ml. 3) The percentages of normal slow waves before, during and after GES were 83.3+/-4.6%, 38.0+/-3.5% and 61.0+/-12.5%, respectively (p=0.02 ANOVA). CONCLUSION: Long-pulse GES at tachygastrial frequency substantially reduces food intake, and is not mediated by the vagal pathway but attributed to relaxation of the stomach and impairment of intrinsic GMA.     

Gastric Electrical Stimulation With Parameters for Gastroparesis Enhances Gastric Accommodation and Alleviates Distention-Induced Symptoms in Dogs

Gastric electrical stimulation (GES) improves symptoms in patients with gastroparesis. We sought to determine if stimulation at fundus with parameters used for gastroparesis could affect gastric accommodation and distention-induced symptoms in dogs. Nine dogs were implanted with a gastric cannula at the anterior stomach and 1 pair of stimulation electrodes in the fundus. Assessment of gastric accommodation and a series of gastric distention were performed using a barostat. Stimulation parameters were of short pulse trains of 14 Hz, 5 mA, 0.3 ms, and 0.1 s on, 5 s off. GES at fundus significantly decreased fasting gastric tone. Fasting gastric volume was significantly increased from 56.3+/-10.4 mL at baseline to 102.4+/-23.1 mL with stimulation (P=.011). Postprandial gastric accommodation was significantly enhanced with stimulation. The extent of accommodation increased from 249.3+/-39.9 mL in the control session to 325.8+/-25.1 mL with stimulation (P=.011). Symptom scores induced by balloon distention of the stomach were significantly lower during stimulation in comparison with those of baseline (P=.016). In conclusion, GES with parameters for gastroparesis enhances postprandial gastric accommodation and reduces visceral perception in normal dogs. This effect, if seen also in humans, may explain in part the symptomatic improvement associated with GES therapy in patients with gastroparesis.     

Two-Channel Gastric Electrical Stimulation Accelerates Delayed Gastric Emptying Induced by Vasopressin

The aim of this study was to investigate the effects of two-channel gastric electrical stimulation (GES) on delayed gastric emptying, gastric dysrhythmias, and motion sickness-like symptoms induced by vasopressin. Seven dogs implanted with four pairs of gastric electrodes and a duodenal cannula were studied in four randomized sessions (saline, vasopressin, single-channel GES, and two-channel GES). The experiment in each session was conducted sequentially as follows: 30-min baseline, ingestion of a liquid meal, 30-min iv infusion of vasopressin or saline, and two 30-min postprandial recordings. In the GES sessions, GES was applied via the first pair of electrodes for single-channel GES or the first and third pairs of electrodes for two-channel GES. Gastric emptying was collected every 15 min via the cannula for a period of 90 min. Results were as follows. (1) Vasopressin induced gastric dysrhythmias, motion sickness-like symptoms, and delayed gastric emptying (P < 0.01, ANOVA). (2) GES normalized gastric dysrhythmias (P < 0.01) but showed no effects on vasopressin-induced emetic response. (3) Two-channel GES improved delayed gastric emptying induced by vasopressin. In comparison with the vasopressin session, two-channel GES, but not single-channel GES, significantly increased gastric emptying at 30 min (43.9 ± 12.6 vs. 27.5 ± 7.7%; P < 0.03), 60 min (75.3 ± 15.1 vs. 54.0 ± 17.8%; P < 0.05), and 90 min (91.6 ± 9.8 vs. 80.3 ± 9.0%; P < 0.05). GES with long pulses is able to normalize gastric dysrhythmias. Two-channel GES improves delayed gastric emptying induced by vasopressin.     

Effect of prepyloric gastric transection and anastomosis on sphincter of Oddi cyclic motility in conscious dogs

Purpose. We previously reported significant changes in sphincter of Oddi cyclic motility after proximal duodenal transection and anastomosis. However, the role of intrinsic myoneural continuity between the antrum and duodenum in this respect is not understood. The aim of this study was to elucidate the effects of prepyloric gastric transection on sphincter of Oddi motility in animals in the conscious state. Methods. Pressures in the bile duct, duodenum, stomach, and sphincter of Oddi and their response to an injection of cholecystokinin-octapeptide were measured in four conscious dogs, with a duodenal cannula, before and after gastric transection and anastomosis 1.5 cm proximal to the pylorus. Results. Gastric transection did not affect the initiation and propagation of the gastroduodenal migration motor complex. Biliary pressure (5.7 ± 0.15 to 5.5 ± 0.2 mmHg; P = 0.91), sphincter of Oddi basal pressure (10.6 ± 0.3 to 10.7 ± 0.2 mmHg; P = 0.97), and amplitude (26.0 ± 1.2 to 32.9 ± 1.7 mmHg; P = 0.304) did not change after gastric transection. Biliary pressure decreased from phase II to phase III of the duodenal migrating motor complex. Cholecystokinin-octapeptide inhibited sphincter of Oddi phasic waves before and after gastric transection. Conclusions. Intrinsic myoneural transection at the prepyloric region does not influence sphincter of Oddi cyclic motility. Preservation of pyloroduodenal myoneural continuity in pylorus-preserving gastrectomy would be beneficial to maintain normal sphincter of Oddi motility. Received: October 30, 2000 / Accepted: February 23, 2001     

Clinical application prospects of gastric pacing for treating postoperative gastric motility disorders

Similar to the heartbeat, gastric peristalsis is regulated by an electrical rhythm generated by a pacemaker. Thus, electrical dysrhythmia of gastric slow waves will inevitably affect gastric peristalsis and emptying. The recurrence of postoperative gastroparesis is thereby closely related to the abnormalities of electrical dysrhythmia and ectopic pacemakers, resulting in postoperatively persistent gastric motility disorders in some severe cases, despite the use of prokinetic and antiemetic drugs. Recent studies have demonstrated that gastric pacing, analogous to pacing the human heart, is an attractive and promising therapy that is both feasible and safe. Gastric pacing has been shown to be strikingly effective in normalizing gastric dysrhythmia, increasing the activity of the gastric slow wave and thereby prompting gastric dynamia and emptying. Furthermore, the long-term utilization of gastric pacing can (i) relieve patients from clinical symptoms, such as nausea and vomiting; (ii) release patients with severe postoperative gastroparesis from relying on prokinetic drugs and the jejunal feeding tube; (iii) return patients to normal oral nutritional intake and provide a more satisfactory nutritional status and most importantly; and (iv) give patients a better quality of life. Overall, research focused on gastric pacing has demonstrated excellent prospects for clinical application in the treatment of postoperative gastroparesis disorders, especially for those unresponsive to prokinetic drugs.     

Inhibitory effects of various types of stress on gastric tone and gastric myoelectrical activity in dogs

Objective. Stress impairs gastrointestinal motility, causing, for example, delayed gastric emptying and altered intestinal transit. However, little is known about the effect of various stress factors on gastric tone and gastric myoelectrical activity (GMA). The aim of this study was to assess the effect of various kinds of stress on gastric tone and GMA in a canine model. Material andmethods. Six dogs, implanted with a gastric cannula and one pair of gastric seromuscular electrodes, were studied. Three kinds of stress (visual, thermal, or audio stimulation) were applied in separate sessions. GMA and gastric tone were recorded for 30 min at baseline and 30 min during stress. Results. Visual stress (blinding) did not alter gastric tone or GMA; cold stress (ice water) and audio stress (loud noise) significantly inhibited gastric tone: gastric volume was increased from 107.2±13.5 ml at baseline to 135.6±23.8 ml with cold stress (p=0.041), and from 106.4±5.7 ml at baseline to 159.2±15.1 ml with audio stress (p=0.007). Although the dominant frequency or power of gastric slow waves was not altered, the percentage of normal gastric slow waves was markedly reduced from 98.3±0.8 to 87.5±3.7 with cold stress and from 90.2±3.3 to 80.6±2.9 with audio stress (p<0.05). Conclusions. Cold- and audio stress inhibit gastric tone and impair gastric slow waves, whereas visual stress does not seem to have such effects. These findings will help to increase our understanding of gastrointestinal motor disorders related to stress.     

Improvement of gastric motility with gastric electrical stimulation in STZ-induced diabetic rats

AIMS: The aims of this study were to observe whether gastric motility was impaired in streptozotocin (STZ)-induced diabetic rats and whether gastric electrical stimulation was able to restore the impaired motility. METHODS: Ten control rats and 30 STZ-induced diabetic rats were used in this study. Gastric slow waves were recorded at baseline and 0, 1, 2, 3 and 4 weeks after the injection of STZ or vehicle. Gastric emptying with (long or short pulses) or without gastric electrical stimulation was measured 6 weeks after STZ injection in a group of 10 diabetic rats each. RESULTS: (1) STZ injection resulted in hyperglycemia and weight loss. (2) Gastric motility was impaired in the diabetic rats. The percentage of normal slow waves was progressively reduced 2 weeks after STZ injection. Compared with the control rats, gastric emptying in the diabetic rats was significantly delayed 6 weeks after STZ injection (60 +/- 3 vs. 79 +/- 2%, p < 0.02). (3) Gastric electrical stimulation with either long or short pulses accelerated gastric emptying in the diabetic rats. (4) Gastric electrical stimulation with long but not short pulses was capable of normalizing gastric dysrhythmia in the diabetic rats. CONCLUSION: Our data show that gastric motility is impaired in STZ-induced diabetic rats as reflected by a progressive reduction in the percentage of normal gastric slow waves and delayed gastric emptying. Moreover, here we show that gastric electrical stimulation normalizes delayed gastric emptying in diabetic rats and this normalization is not attributed to the effect of gastric electrical stimulation on gastric slow waves.     

胃电刺激对顺铂诱导的犬呕吐症状的影响

目的 研究顺铂(cisplatin,DDP)对胃肌电活动的影响,并探讨胃电刺激(GES)对化疗药物引起的犬呕吐和消化不良症状的治疗效应.方法 7只比格犬的胃浆膜均被植入4对电极,每只犬均先后进行两阶段实验.(1)DDP阶段:给予DDP(1.5 mg/kg),自给药开始持续记录胃电活动及动物症状;(2)GES+DDP阶段:自DDP给药开始,经近端胃体部电极持续给予串脉冲GES,给药剂量、胃电活动及症状记录同DDP阶段.结果 (1)DDP能诱导犬恶心呕吐症状及胃电紊乱:DDP阶段动物均出现频繁呕吐,呕吐次数为(5.5±1.2)次,总症状评分为31.83±2.75.通过胃电记录发现,基线水平时正常胃慢波占(96.50±1.14)%,而呕吐期间正常胃慢波占(69.61±5.81)%(P=0.003),并且胃电过速和胃电过缓发生的百分比均明显高于基线水平(P=0.020和P=0.031).(2)GES能减轻DDP诱导的呕吐和消化不良症状:GES+DDP阶段比格犬的症状评分较DDP阶段明显降低(24.50±1.45比31.83±2.75,P=0.028),并且呕吐次数也明显减少(3.7±0.8比5.5±1.2,P=0.028).但GES对DDP引起的胃电紊乱无明显影响.结论 DDP能诱导犬呕吐和胃电紊乱.串脉冲GES能明显减轻DDP引起的呕吐和消化不良症状,但对胃电紊乱无明显影响.     

Origins and patterns of spontaneous and drug-induced canine gastric myoelectrical dysrhythmia

The aim of this study was to investigate the characteristics and orientation of gastric dysrhythmia using multichannel serosal recordings in dogs. Ten dogs chronically implanted with four to eight pairs of electrodes were studied. Gastric slow waves were recorded in four sessions: postsurgical and after atropine, vasopressin, and glucagon. A total of 554.7 min of bradygastria, 201 min of tachygastria and 22.3 min of arrhythmia were observed in the recordings. The majority of bradygastria (80.5 ± 9.4%) originated in the proximal stomach (P < 0.04, vs other locations) and propagated all the way to the distal antrum. In contrast, tachygastria mainly originated in the distal antrum (80.6 ± 8.8%) (P < 0.04, vs other locations) and propagated partially or all the way to the proximal stomach. Dysrhythmia appeared intermittently with normal gastric slow waves. In all recordings, normal slow waves were present 38.0 ± 5.3% of the time, while bradygastria, tachygastria, and arrhythmia were present 35.9 ± 5.3%, 23.0 ± 1.6%, and 2.4 ± 0.5% of the time, respectively. The prevalence of dysrhythmia was highest in the distal antrum (80.4%) (P < 0.01) and lowest in the proximal part of the stomach. In conclusion, tachygastria originates from an ectopic pacemaker in the distal antrum. It may completely or partially override the normal slow waves. Bradygastria is attributed to a decrease in the frequency of the normal pacemaker in the corpus. The prevalence of gastric dysrhythmia is different in different locations of the stomach and is highest in the distal antrum.